gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Platelet Serotonin is Involved in Hypertensive Target Organ Damage

Serotonin in Blutplättchen ist an der Entstehung hypertensiver Endorganschäden beteiligt

Meeting Abstract (Hypertonie 2004)

  • C.S. Wilhelm - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)
  • L.A. Campos - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)
  • O.C. Baltatu - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)
  • V. Gross - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)
  • D.J. Walther - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)
  • M. Bader - Max-Delbrück-Centrum für Molekulare Medizin (MDC), Max-Planck-Institut für Molekulare Genetik (Berlin, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP35

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2004/04hoch035.shtml

Veröffentlicht: 10. August 2005

© 2005 Wilhelm et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Besides being a prominent neurotransmitter serotonin is also a cardiovascular hormone with potent actions on endothelial and vascular smooth muscle cells as well as cardiomyocytes. We have recently established mice lacking tryptophan hydroxylase (TPH) 1, the rate-limiting enzyme in serotonin synthesis. These animals lack serotonin in the blood, in particular in the platelets, but exhibit normal levels of the hormone in the central nervous system due to the presence of the previously unknown neuronal isoenzyme, TPH2. These mice are ideal models to study the cardiovascular functions of serotonin. We could show that TPH1 knockout (KO) mice show an impaired hemostasis due to attenuated secretion of von-Willebrand factor from platelets. In order to analyze the effects of platelet serotonin on hypertensive end-organ damage, we treated these mice with DOCA/salt. TPH1-KO mice on C57Bl/6 background and controls did not differ in their basic blood pressure values measured by telemetry and both groups developed increased mean arterial pressures after three weeks of DOCA/salt treatment. However, cardiac hypertrophy induced by DOCA/salt treatment was with 143% of basal cardiac weight significantly (p<0.005) more pronounced in the mice lacking peripheral serotonin than in control mice with 123%. Furthermore, albumin excretion into the urine as a marker for kidney damage was 7 times higher in TPH1-KO mice and histological sections confirmed the exaggerated renal damage in these mice. In conclusion, serotonin in platelets protects animals from target organ damage induced by DOCA/salt treatment. Actions of peripheral serotonin on the immune system, for which we also have evidence from studies in TPH1-KO mice, may be involved in these effects.